The present invention relates to a nutritional intervention composition for enhancing satiety prior to the consumption of a meal resulting in reduced caloric intake during the meal, and lengthening the inter-meal interval by extending satiety for up to three and a half hours following the meal. More particularly, the nutritional intervention composition includes a protein source, caseinmacropeptides or glycomacropeptides or any hydrolysis product of GMP, long chain fatty acids and soluble and/or insoluble fibers. By extending the feeling of satiety, the nutritional intervention composition decreases food intake producing weight loss over time. The composition can be taken prior to a meal or can be mixed with food to extend the satiation effect of that food.
The present invention also relates to a nutritional intervention composition to help individuals with Type II diabetes maintain glycemic control and extend satiety. By extending the feeling of satiety, the nutritional intervention composition decreases food intake resulting in a decrease in body weight over time while providing better regulation of glucose and insulin levels following consumption of a meal. Furthermore, since CCK causes a delay in stomach emptying, the nutritional intervention composition can slow the absorption of glucose by the small intestine further improving glycemic control.
The present invention also relates to a nutritional intervention composition designed as an adjunct to treat patients with bulimia and eating disorders who have been shown to have a defect in their satiety control mechanisms. By stimulating satiety before a meal and extending satiety after a meal, the present invention reduces binge eating in bulimic patients.
1. Background of the Invention
Satiety
Cholecystokinin (CCK) is a peptide released following the consumption of food. The literature demonstrates an injection of CCK in animals elicited the total range of satiety behavior.
Release of cholecystokinin has also been shown to be a satiety signal in humans. In 1981, researchers showed that an injection of CCK decreased food intake by 16 percent. The subjects did not alter their rate of eating but rather stopped eating earlier, which would be the expected results if cholecystokinin were a satiety signal. The results in humans confirmed the results in the laboratory that CCK is an important agent in terminating the meal. Although the full mechanism whereby CCK exerts its effect on satiety is not known, there appears to be two components, a central component involving CCK receptors in the brain and a peripheral component involving the stomach and small intestines.
When food is consumed, CCK releasing protein (CCKRP) is released in the small intestine. CCKRP stimulates CCK release from intestinal cells. The release of CCK generates the behavioral symptoms associated with satiety and at the same time activates a number of negative feedback mechanisms to turn off the CCK response. There are primarily two negative feedback mechanisms, one involving proteases secreted by the pancreas and the second bile from the gallbladder. CCK stimulates the pancreas to secrete a number of proteases, specifically trypsin and chymotrypsin, which inactivate CCKRP. CCK also stimulates gallbladder contraction causing bile acids to be released into the intestinal lumen. Bile acids are powerful regulators of CCK, inhibiting its release.
The literature has also shown that CCK release can be stimulated by protein such as whey and casein, hydrolysis products of casein including glycomacropeptide, phenylalanine, calcium and long chain fatty acids. All of the literature to date has shown that regardless of how CCK is stimulated or what intervention is taken to prevent its breakdown, its reported effect is on the termination of the meal.
It has been well documented that some soluble and insoluble fibers as well as plant saponins bind bile salts. In fact, it is the binding of bile salts by fiber, which is believed partly responsible for the hypocholestrolemic effect of these agents. Different fibers have different binding capacities to the various bile salts. For instance, cellulose has been shown to bind bile acids poorly.
The ability of CCK to reduce appetite would appear to make it an extremely useful agent in treating obesity. In a weight management program, stimulation of CCK would result in less food consumed and reduction of hunger cravings between meals. These effects would enable an overweight individual to better comply with a diet that has a reduced caloric intake. The major limitation in the use of CCK, as an appetite control agent, is that it must be given by injection. Additionally, CCK release initiates a number of negative feedback mechanisms described above involving the pancreas and gallbladder that terminate the CCK response.
There is a definite need in the art for a nutritional intervention composition that can be taken orally to permit a subject to be satiated with a lower caloric intake. There is also a definite need in the art for a nutritional intervention composition that not only can be taken prior to a meal to stimulate satiety before the meal but whose properties extend satiety following the meal thereby lengthening the inter-meal interval.
There is also a definite need in the art for a nutritional intervention composition that can be taken orally and that with a total caloric value of only 80 calories can strongly provoke satiety.
Glycemic Control
It is well known the art that slowing gastric emptying can blunt the post-prandial rise in glucose and insulin. Most persons with Type II diabetes are obese and have an inability to respond normally to insulin. Obesity is a major contributing factor to the development of Type II diabetes. The primary treatment for Type II diabetics is diet and a weight loss program. Dietary guidelines for Type II diabetics include consumption of fiber. Fiber has been shown to slow gastric emptying. One of the prominent effects of cholecystokinin is also to delay gastric emptying. The ability of fiber and cholecystokinin to delay gastric emptying are well known in the art and the result of delayed gastric emptying is to slow the absorption of glucose.
There is a definite need in the art for a nutritional intervention composition that can be taken orally by Type II diabetics that stimulates the release of CCK in a calorically efficient way, and that permits Type II diabetics to be satiated with a lower caloric intake and offers a better degree of glycemic control.
There is a definite need in the art for a nutritional intervention composition that not only can be taken prior to a meal to stimulate satiety before the meal but whose properties extend satiety following the meal thereby lengthening the intermeal interval in order to help the Type II diabetic lose weight.
Bulimia
Bulimia is an eating disorder that usually effects females. A major characteristic of bulimia is an inability to become satiated by food. As a result bulimics tend to binge on food and regurgitate it to prevent weight gain. This disorder is classically treated with psychotherapy. Studies have shown that bulimics have a defect in their normal satiety mechanisms. They release less CCK following a meal.
There is a definite need in the art for a nutritional intervention composition that can be taken orally by bulimics, and is a calorically efficient stimulator of CCK to permit bulimics to be satiated. An important element of this invention is the design of a product that not only can be taken prior to a meal to stimulate satiety before the meal but whose properties extend satiety following the meal thereby lengthening the inter-meal interval.
2. Description of the Prior Art
Satiety
U.S. Pat. No. 4,833,128 discloses the oral administration of phenylalanine in conjunction with protein, carbohydrate and fat to stimulate satiety. This invention teaches that when a dietary supplement containing phenylalanine is consumed fifteen minutes prior to a meal, it generates a feeling of satiety resulting in less food consumption at the subsequent meal. The CCK release slows gastric emptying and the fiber in the invention provides an additional effect by slowing gastric emptying. The nutritional supplement in this patent contains 140 calories and it is recommended that it be taken three times a day. At a dose of three times a day this dietary supplement would provide almost 25% of the total calories suggested in a reduced caloric program (1600 calories) to lose weight. Furthermore, the addition of phenylalanine limits its use in patients with phenylketonuria. The invention also teaches that cellulose should be added. Cellulose has been shown to be one of the poorest binders of bile acids and therefore would not stimulate satiety by blocking the effect of bile acids and salts on cholecystokinin release. Finally, the invention does not have any effect on extending the duration of action of CCK. In fact, the invention teaches that the appetite suppression of CCK may be merely temporary resulting in a limited satiety effect.
U.S. Pat. No. 4,491,578 discloses the oral administration of a trypsin inhibitor to enhance satiety by stimulating the release of CCK. This patent teaches that the negative feedback signal for cholecystokinin secretion results from the release of trypsin from the pancreas. The administration of a therapeutically effective quantity of trypsin inhibitor blocks the trypsin released from the pancreas thereby interfering with a negative feedback mechanism. The nutritional intervention composition described in this application does not depend on trypsin inhibition for its effect on satiety.
U.S. Pat. No. 5,932,561 teaches that dietary supplements that bind lipids can aid in weight loss and reduce cholesterol. The patent also teaches that a dietary supplement composition that contains saponins from aloe increase the capacity of chitosan to bind fat. The saponins also act as a laxative to off set the constipating effects of chitosan. This patent does not teach that either chitosan or saponins can be used to stimulate cholecystokinin. The weight management characteristics of this invention are to primarily combine fat and cholesterol and remove it from the body.
U.S. Pat. No. 5,703,052 teaches that saponins are useful in controlling hypercholesterolemia. This patent does not describe the use of saponins as a stimulator of CCK.
Glycemic Control
U.S. Pat. No. 5,187,154 teaches that Type II diabetics exhibit more rapid gastric emptying than normal controls in the early stages of their diagnosis and that an invention that can slow gastric emptying will improve glycemic control. The patent also teaches that the invention is useful for assessing the risk of diabetes in subjects who do not show any abnormalities in glucose metabolism. The patent utilizes a therapeutic dose of trypsin inhibitor to stimulate CCK release and thereby slow gastric emptying which in turn results in improved glycemic control. The nutritional intervention described in the present invention does not depend on trypsin inhibition for its effect on glycemic control.
None of the prior art patents disclose the nutritional composition of the present invention for enhancing and extending satiety with a calorically efficient preparation.
Accordingly it is an object of the present invention to provide a nutrition intervention composition for enhancing satiety before a meal.
Another object of the present invention is to provide a nutrition intervention composition to extend satiety after a meal.
Another object of the present invention is to provide a nutrition intervention composition that can be consumed prior to a meal to enhance satiety.
Another object of the present invention is to provide a nutrition intervention composition that can be added to food to extend the satiating effect of the food to which it is added.
Another object of the present invention is to provide a nutrition intervention composition to stimulate cholecystokinin release in a calorically efficient manner.
Another object of the present invention is to provide a nutrition intervention composition to increase cholecystokinin by stimulating its release through a combination of nutritional agents.
Another object of the present invention is to provide a nutrition intervention composition to stimulate cholecystokinin release by binding to bile salts.
Another object of the present invention is to provide a nutrition intervention composition to cause weight loss resulting from a reduced caloric intake.
Another object of the present invention is to provide a nutrition intervention composition to provide better glycemic control for Type II diabetics.
Another object of the present invention is to provide a nutrition intervention composition to help Type II diabetics enhance and extend satiety in a calorically efficient fashion.
Another object of the present invention is to provide a nutrition intervention composition to increase satiety in bulimics who have a defect in their normal CCK release mechanism.
Another object of the present invention is to provide a nutrition intervention composition to help in the management of the bulimic patients.
Another object of the present invention is to provide a nutrition intervention composition that is palatable, well tolerated and without side effects to individuals.
In brief this invention relates to a nutritional intervention composition in a dry power form for enhancing satiety prior to a meal and extending satiety after a meal in a calorically efficient fashion. The dry nutritional composition includes protein, caseinmacropeptides (CMP) or glycomacropeptides (GMP) or any hydrolysis product of GMP, long chain fatty acids, soluble and/or insoluble fibers. The dry nutritional composition includes protein in the range of 0.21% to 88.30%, glycomacropeptide in the range of 0.05% to 87.72%, oleic acid in the range of 2.27% to 97.25%, soluble fibers in the range of 0.19% to 79.05%, and insoluble fibers in the range of 0.19% to 79.05%. The composition may also include plant saponins, calcium and cholestyramine.